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1
Q

What percentage of childhood deaths (kids under 5 are caused by diarrhoea)?

A

about 11%

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2
Q

Describe the two ways in which diarrhoea kills?

A

Immediate: due to a fluid and electrolyte imbalance
Delayed: mainly due to malnutrition

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3
Q

What is the association between diarrhoea and malnutrition?

A

It causes increased energy loss. This is due to diarrhoea, vomiting and increased metabolic needs.

Reduced energy intake. When the gut is inflamed food is malabsorbed.
An additional problem is that when kids have diarrhoea and malnutrition mothers (mainly in the 3rd world) think that it has something to do with the milk/food that the kids are eating and withhold it, this is very dangerous

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4
Q

How much fluid goes through the gut and how much is reabsorbed in 24 hours?

A

10L in
9.9L reabsorbed
About 100ml comes out in faeces

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5
Q

In L how much fluid is secreted by each of the regions of the GIT?

A 
Mouth 2L (eg from food and drink)
Salivary glands 1.5L 
Stomach 2.5L
Liver (bile) 0.5L
Pancreas 1.5L
Small bowel 2.0L
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6
Q

What is the reserve capacity of the colon?

A

The colon can absorb up to 6 litres if needed (i.e. if a person has diarrhoea which comes from the small intestine)

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7
Q

Does diarrhoea come from the small or large intestine?

A

Both

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8
Q

What is the primary cause of diarrhoea in developed and developing countries?

A

Developed - viral

Developing - bacterial

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9
Q

What is Gastroenteritis?

A

Gastroenteritis - inflammation of the intestines and the stomach

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10
Q

What is the most common cause of ‘gastro’

A

Non specific

- no defined cause could be virus bacteria or protozoa (never fully investigated)

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11
Q

What is the causative agent of dysentery?

A

Shigella/EIEC, protozoa (Entamoeba histolytica)

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12
Q

What are the main foodborne causes of diarrhoea?

A

Salmonella, Vibrio, Listeria, Yerisinia, Cmpylobacter, EHEC viruses, Clostridium, Bacillus, Ciguatoxin etc

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13
Q

What is the most common cause of food borne diarrhoea in Aus?

A

Salmonella

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14
Q

What happens when clostridum perfinges is ingested?

A

It is normally found in spore form, when it enters the gut it sporylates and can release its toxin

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15
Q

where is Ciguatoxin found?

A

It is found in fish and can be very dangerous (it can kill)

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16
Q

What is travellers diarrhoea?

A

People become immune to infectious agents to the immediate area - if you go to visit places later in life are not immune to pathogens in the water/area

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17
Q

What are some causes of travellers diarrhoea?

A

ETEC, other bacteria, viruses, protozoa

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18
Q

What is colitis?

A

Inflammation of the colon

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19
Q

What is the causative agent of pseudomembranous colitis?

A

Clostridium difficile
The colitis is thought to occur when this bacterium replaces normal gut flora that has been compromised, usually following antibiotic treatment for an unrelated infection. The disturbance of normal healthy bacteria may provide C. difficile an opportunity to overrun the intestinal microbiome. It is a type of antibiotic-associated diarrhea.

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20
Q

When does pseudomembranous colitis occur?

A

thought to occur when this bacterium replaces normal gut flora that has been compromised, usually following antibiotic treatment for an unrelated infection. The disturbance of normal healthy bacteria may provide C. difficile an opportunity to overrun the intestinal microbiome

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21
Q

What are the causative agents of cholera-like diarrhoea?

A 
Vibreo cholerae (If an epidemic of Cholera is suspected, the most common causative agent is V. cholerae O1. If V. cholerae serogroup O1 is not isolated, the laboratory should test for V. cholerae O139) 
ETEC
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22
Q

What is enteric fever?

A

Typhoid fever is a type of enteric fever along with paratyphoid fever.

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23
Q

What are the classic symptoms of non-specific gastro?

A

Loose stool. Not watery

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24
Q

What are the classic symptoms of dysentery?

A

Blood, pus and mucous in stool (Associated with invasive bacteria)

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25
Q

What are the classic symptoms of cholera-like diarrhoea?

A

Very watery gastro

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26
Q

What are the classic symptoms of enteric fever?

A

is a type of septicaemia, those infected are sick with a host of symptoms for a number of weeks.

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27
Q

What are the 5 pathotypes of diarrhoeagenic E. Coli

A 
Enterotoxigenic E. coli (ETEC)
Enteropathogenic E. coli (EPEC)
Enterohemorrhagic E. coli (EHEC)
Enteroinvasic E. coli (EIEC)
Enteroaggregative E. coli (EAEC)
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28
Q

What are the symptoms of ETEC?

A

Watery diarrhoea

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29
Q

What are the symptoms of EPEC?

A

Non-specific gastro

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30
Q

What are the symptoms of EIEC?

A

Dysentry

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31
Q

What are the symptoms of EHEC?

A

Bloody diarrhoea

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32
Q

What are the symptoms of EAEC?

A

Watery diarrhoea

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33
Q

Who is most at risk of contracting ETEC?

A

Infants in LDs; travellers

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34
Q

Who is most at risk of contracting EPEC?

A

Children in LDCs

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35
Q

Who is most at risk of contracting EIEC?

A

Any age, mainly in LDCs

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36
Q

Who is most at risk of contracting EHEC?

A

Any age developed countries

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37
Q

Who is most at risk of contracting EAEC?

A

Children in LDCs

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38
Q

What are the adhesins and toxins of ETEC?

A 
A = CFAs
T = Enterotoxins
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39
Q

What are the adhesins and toxins of EPEC?

A 
A = Intimin, Bfp
T = T3S effectors
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40
Q

What are the adhesins and toxins of EHEC?

A 
A = Intimin, Efa
T = Shiga toxins
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41
Q

What are the adhesins and toxins of EIEC?

A

A =IpaC etc.

T = ShET

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42
Q

What are the adhesins and toxins of EAEC?

A 
A = AAF
T = Pet, EAST
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43
Q

What is the MOA of ETEC?

A

Heat Labile Enterotixin of ETEC = same action as cholera toxin

1) Toxin binds via B on membrane.
2) Retrograde vesicular transport through Golgi/ER -> release of A1 subunit ->
3) activation of Adenyl CycalseC  increase in cAMP ->
4) activates CFTR (Cl- channel)
5) Cl- efflux from cells in SI and NaCl influx blockade in villus ->
6) accumulation of electrolytes in lumen as CL and Na are in the lumen.
7) -> diarrhoea.

Heat Stable:

1) Binds and activates GC -> accumulation of cGMP in gut.
2) Leads to Cl- efflux from si CELLS, and NaCl blockade at the villus  electrolyte accumulation in intestinal lumen -> diarrhoea

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44
Q

Do ETEC invade the GIT?

A

Colonise but do not Invade.

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45
Q

MAO of EPEC

A

Stage 1:
• Initial adherence via Bundle forming Pili and attach to intact Microvilli. (plasmid encoded).
Stage 2:
• Lose Microvilli (effaced -> very intimate attachment of EPEC to the effaced enterocytes.
• This morphological change is ass with the original binding by the BFP activating a series of genes encoded on a pathogenicity island called LEE (encodes genes that enable tight binding).

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46
Q

MAO of EHEC

A 
Shiga toxin (Stx): 
1.	B subunit binds to Gb3
2.	 -> retrograde transport via vesicle through Golgi/ER 
3.	-> A1 subunit activated and binds to 28S rRNA of 60S subunit 
4.	-> inhibits translation.
•	Gb3 found on endothelial cells:
(i)	lamina propria, 
(ii)	glomerulus (renal problems), 
(iii)	pancreas (diabetes), heart, 
(iv)	Brain.

II

  1. EHEC ingested in food/water
  2. Attach to intestinal mucosa (e.g. using LEE PI).
  3. Produce Shiga toxin (cytotoxic)
  4. Toxins absorbed from gut intact  binds Gb3 on En cells  damage BVs supplying gut, kidney etc.
  5. HUS occurs when endothelial damage stimulates the coagulation cascade  fibrin clots  haemolysis of RBCs together with organ damage (kidney, pancreas, heart, brain).
  6. EHEC is most common cause of paediatric renal failure.
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47
Q

MOA of EIEC

A
  1. Only E. coli that INVADES enterocytes! Invades enterocytes of LI
  2. Spread to adjacent cells  INFLAMMATION
  3. EIEC & Shigella only invade to mucosa. Salmonella typhi invades to blood.
  4. Induce damage, ulceration, inflammation  dysentery.
  5. V similar to shigella. Shigella invades and may release shiga here which can get in and do what it did in EHEC
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48
Q

MAO of EAEC

A
  1. Characteristic pattern of adhesion to SI
  2. Cause of persistent diarrhoea
  3. EAEC lie down on enterocyte surface and stack themselves up like bricks.
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49
Q

What does EHEC bind to?

A

Binds to endothelial cells not enterocytes

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50
Q

Name 2 adhesive enterotoxigenic diarrhoea causing bacteria:

A

cholera and ETEC

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51
Q

Name a bacteria which adheres to the brush border and causes damage

A

EPEC

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52
Q

Name a bacteria that restricts its invasion to the mucosa?

A

Shigella

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53
Q

Name 2 bacteria which invade the submucosa:

A

Salmonella and Campylobacter

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54
Q

Which bacteria invades systematically?

A

Salmonella

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55
Q

Why doesn’t EIEC need such a well defined colonisation system?

A

They colonise the large intestine where food moves slower, thus it does not need high powered grappling hooks to hang on.

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56
Q

what are the 4 virulence factors?

A

Adehesins
Exotoxins
Invasive ability
Ability to resist killing

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57
Q

What is an adhesin?

A

Fimbria/intimin in non frimbreate

58
Q

What are the two types of exotoxins and which bacteria produce them?

A

Cytotonic - cholera toxin, LT and ST of ETEC

Cytotoxic - Shiga toxin (produced by EHEC)

59
Q

Give an example of the invasive ability of two different bacteria.

A

Shigella and EIEC carry invasion plasmids which help them penetrate tissues + spread from cell to tell within the mucous

60
Q

What are the two ways in which bacteria are able to resist killing?

A

By serum
By phagocytosis
Important for facultative intracellular pathogens, or those that invade tissue widely such as Yersinia or Salmonella: by serum – Yersnia, by phagocytes - Yersinia, Salmonella

61
Q

Under what circumstances would one want o make a lab diagnosis of the pathogen causing diarrhoea?

A

If it is persistent (more than 2 weeks)
If it it bloody
If it is a young child
If a person is immunocompromised

62
Q

What are the 5 techniques used to make a lab diagnosis of bacteria?

A 
Macroscopic appearance 
Microscopy
Culture
Antigen detection
Detection of nucleic acid (viruses, bacteria and protozoa)
63
Q

What cause of diarrhoea can be detected by its macroscopic appearance alone?

A

Dysentery - watery?

64
Q

What are we usually looking for in lab diagnoses using antigen detection?

A

viruses, parasites, toxins

Rotavirus, giardia, shiga toxin

65
Q

What produces shiga toxin?

A

Shiga toxin is produced by some strains of Shigella dysenteriae and by all strains
of enterohaemorrhagic E. coli (EHEC).

66
Q

What causes bacillary dysentery?

A

Enteroinvasive E. coli (EIEC) carries nearly identical virulence determinants to
Shigella species and causes the same type of clinical syndrome, namely, bacillary
dysentery.

67
Q

what are some other names for shiga toxins?

A

Shiga toxins are also known as Shiga-like toxins and Verotoxins.

68
Q

What are the two types of dysentery?

A

Amoebic and bacillary

69
Q

What is the life cycle of Giardia lamblia?

A

Life cycle of Giardia lamblia
- Ingestion of dormant cysts
- Excytation - trophozites emerge in an active from
- Trophozoite undergo asexual reproduction
- Exit symptoms
- Encystation - during transit towards the colon (if the trophozoites are visible it means they past to quickly through the GIT and didn’t have time to form cysts
- Cysts and trophozoites expelled in faeces
- Only cysts can survive outside of the host
Cyst can survive for weeks to months in cold water and then enter into another body

70
Q

If giardia are detected in the stool are they the definitive cause of diarrhoea?

A

• trophozoites; normally inhabit the small intestine (duodenum); can be flushed out by another cause of diarrhoea therefore isolation does not necessarily mean it is the cause of diarrhoea

71
Q

What does Entamoeba cause?

A

It cuases amoebic dysentery and stimulates an inflammatory response resulting in RBS in stool

72
Q

What are the limitations in using the various diagnosis methods for viruses?

A

Astrovirus, coronavirus, rotavirus, norovirus etc. = easily visualized in faeces + detected by enzyme immunoassay or PCR BUT almost none of the viruses can be grown in culture; VERY difficult to grow

73
Q

How are Cryptosporidium sp (yeast GIT pathogens) detected?

A
  1. antigen detection in immunoassay

2. modified ZN stain

74
Q

How are faces enriched?

A

Salmonella is the most common which is easy to find

- Enrichment - grown in a broth which favours salmonella or one which disadvantages the other cells 
- If there is no obvious signs on the original plate they can then plate the growth from the broth

This broth is only routinely done for salmonella NEED TO ASK FOR OTHER BACTERIA (can make other broths - i.e. with other growth factors)

75
Q

Without using the enrichment process how else can one culture faeces to look for a pathogen of interest?

A

Direct plating on selective/indictor media
Confimation of suspoicious colonies is done using
biochemical tests and serotyping/pathotyping (by PCR, as necessary)

76
Q

What is antigen detection for diagnosis of viral infections?

A

Eg Rotavirus
Antibody to rotavirus on solid phase (usually latex beat) add patients faeces, wash away all the junk, only thing which stays is rotavirus, add second specific antibody

77
Q

What is detection of nucleic acid for detection for diagnosis of viral infections?

A
  • Amplification by PCR -> electrophoresis
  • Identification by 1) RFLP 2) hybridization 3) sequencing
  • Eg. norvovirus
78
Q

What is Electron microscopy for detection for diagnosis of viral infections?

A

Visualised under an electron microscope
**rotavirus has triple capside around it – protects against stomach acid.
Adenovirus serotype 40 and 41 can sometime be grown from feacesbut cannot be observed under EM

79
Q

Are gastroenteritic pathogens easy to grow in the lab?

A

NO which is a bit of a paradox, i.e. if you can grow it it is unlikely to be the causative agent.

80
Q

What is appropriate treatment of diarrhoea?

A

1) Replace fluid and electrolytes
• intravenous • oral
2) Reduce fluid loss

81
Q

How are fluids and electrolytes replaced?

A

Using oral re-hydration salts which contains a solutes.
The Na+/Cl- transporters are inactive during diarrhoea and as such water does not follow as there is no osmotic gradient. However the Solute/Na+ transporter is still functional thus adding glucose (as the solute) allows the creation of an osmotic gradient for water to follow (plus the absorption of Na+)

82
Q

What are the methods used to reduce fluid loss?

A 
1)  Anti-diarrhoeals 
• anti-motility agents 
• anti-secretory agents 
• binding agents
2) Antimicrobials
83
Q

Should antimicrobials be used in the following:
• Cholera
• Systemic infections, e.g. typhoid fever
• Immunocompromised patients
• Severe infections with Shigella
• Protozoal infections
• Pseudomembranous colitis

A

• Cholera
May be effective in cholera - reduce spread. It needs to culture

• Systemic infections, e.g. typhoid fever
Have to use antimicrobials 3rd generation cephelasporin

• Immunocompromised patients
Should use antimicrobial also for those who are malnourished

• Severe infections with Shigella
These should be treated, but the strains often have resistance

• Protozoal infections
Always treat even if asymptomatic, commonly use an agent like metromitozol

• Pseudomembranous colitis
Would start off with metromitozol (acts only on anearobic agents) if that fails we would treat with vancomycin - worried about vancomycin resistant enteroccoci - which can make Vancomysin resistant staph aureus

84
Q

What does the WHO Diarrhoeal Disease Control Program involve?

A
  • Reduce diarrhoea-associated mortality
  • Reduce incidence of diarrhoea through:
  • education: hygiene, breast-feeding, etc.
  • immunisation
85
Q

What are the measures one can take to prevent travellers’ diarrhoea?

A

Reduce exposure to infectious agents (drink bottled or re-boiled water)
Antimicrobials (should be weary, excessive use has led to resistance)
Immunisation

86
Q

What is a side effect of tetracyclines which may make it unpleasant to travellers?

A

Increased sensitivity to sunlight

87
Q

Name 3 ectoparasites

A

Lice • Mites • Ticks

88
Q

Name 3 protozoal parasites

A

• Entamoeba histolytica • Giardia intestinalis • Toxoplasma gondii

89
Q

What is a definitive host?

A

Host in which the parasite reaches sexual maturity

90
Q

What is an intermediate host?

A

Host in which development occurs but the parasite does not reach sexual maturity

91
Q

What is a paratenic host?

A

Host in which the parasite enters the body and does not undergo development but remains infective

92
Q

What is a reservoir host?

A

An animal which can be normally infected with a parasite that also infects people

93
Q

What is the definition of a parasite?

A

A plant or animal that lives on or in another living organism on which it is METABOLICALLY dependent

94
Q 
Classify the following
Flies and mosquitos 
Ticks
Lice
Mites
Fleas
A

• Insects
Flies and mosquitos – Fleas – Lice

• Arachnids
Mites – Ticks

95
Q

What are the three types of lice?

A

Lice have a very focussed ecological niche - i.e. one specific type of hair/bird etc.

P. humanis – body louse, clothing spread, causes infestation of body hair

P. capitis – head louse, spread by contact, causes a head itch

P. pubis – ‘crabs’, spread by contact, similar life cycle to capitis but only lives on pubic hear - pubic hair is oval whilst on the head it is round

There has been an upsurge worldwide in head lice but pubic lice has decreased significantly

96
Q

What causes the itch in lice?

A

The saliva the louse uses to attach

97
Q

Life cycle of louse

A 
Emerges after 6-7 days form an egg
Moults 3 times over the next 9 days 
Mating occurs
Eggs are laid over next 13 days
Louse dies after 32-35 days
98
Q

Lice

  1. Distribution
  2. Symptoms
  3. Diagnosis
  4. Treatment
  5. Disease control
  6. Significance
A
  1. Worldwide
  2. Ithc, macules (discoloured area of skin), 2nd deg infection
  3. Detection of eggs
  4. Topical insecticides (likely will see resistance)
  5. Treat infected people
  6. Stigma, vectors of rickettsia (typhus, trench fever) and spirochetes
99
Q

Where do mites live?

A

Live in tunnels in epidermis (fingerwebs, elbows, axillae, genitals) - it is small (less than 0.5mm which allows it to do this.
Its life cycle is on a single host
They are spread by contact

100
Q

What is the life cycle of mites (scabies)?

A

Adult deposits eggs as they burrow into skin
Larvae moult into nymphs, Larvae and nymphs are found in short burrows called molting pouches.
Mating occurs after the male penetrates the molting pouch of the adult female
Impregnated females then extend their pouches into burrows laying eggs along the way

101
Q

Scabies

  1. Distribution
  2. Symptoms
  3. Diagnosis
  4. Treatment
  5. Disease control
A
  1. Worldwide
  2. Itch, dermatitis
  3. Detection of mite in scrapings/biopsy
  4. Ivermectin (single dose), topical scabicides
  5. Treat infected people, sterilize clothes/bedding (mites can survive for some time outside of the body)
102
Q

Ticks paralysis - Ixodes holocyclus

  1. Distribution
  2. Symptoms
  3. Diagnosis
  4. Treatment
  5. Disease control
A
  1. Eastern Aus (others worldwide)
  2. Rapid ascending paralysis
  3. Detection of tick
  4. Removal of tick (physical examination is key)
  5. Clothing, repellent, examination of body surfaces after potential exposure
103
Q

Why are ticks of significant concern?

A

They are vectors of infectious agents (viral, rickettsial, bacterial, protozoal) • Some may cause paralysis

104
Q

What are the two forms of protozoa?

A
  • Cystic (resistance stage which can survive outside of host)
  • Trophoziate (active and invasive pathogen
105
Q

How do protozoa cause pathology?

A
  • Associated with proliferation within the host

* Pathogenicity varies greatly, affected by host and parasite factors

106
Q

How does Entamoeba Histolytica infect and spread?

A
  • Trophoziates invade tissues in colon
  • Faecal-oral transmission
  • May cause extra-intestinal infection (in liver, brain)
  • Can cause abscess in liver/ brain

It is the most frequent cause of protozoal disease in humans

107
Q

Amoebiasis

  1. Distribution
  2. Symptoms
  3. Diagnosis
  4. Treatment
  5. Disease control
  6. Immunity
A
  1. Worldwide
  2. Prolonged watery diarrhoea, liver abscess
  3. Faecal cysts, serology
  4. Metronidazole + paromomycin, drainage of abscess
  5. Clean water, sewage treatment
  6. Reinfection is common.
108
Q

How does Giardia intestinalis infect and spread?

A
  • Flagellate, primitive eukaryote
  • Two life forms: trophozoites and cysts
  • It is spread throught the faecal-oral route and through zoonotic transmission
  • No systemic inflamm response as Giardia doesn’t enter blood
109
Q

Giardiasis

  1. Distribution
  2. Symptoms
  3. Diagnosis
  4. Treatment
  5. Disease control
  6. Immunity
A
  1. Worldwide (possums are hosts in Aus)
  2. Diarrhoea, may be acute or chronic, malabsorption - symptoms can persist for months. In the acute phase it can cause bloody diarrhoea
  3. Cysts in faeces
  4. Tinidazole (sometimes given to travellers before going to areas where it is endemic)
  5. Clean water, sewage treatment
  6. Re-infection is common
110
Q

Infection and spread of toxoplasma gondii:

A
  • Obligate intracellular parasite and infects all mammals (esp cats)
  • Most infections acquired from eating poorly cooked meat;
  • Infection persists for life
  • Infections occurs in muscle and brain.
111
Q

Name 3 situations in which one needs to be careful with toxoplasma gondii?

A
  1. Transplant
    Screening of both the donor and host should be undertaken before transplantation, it can be dangerous to the immunosuppressed
  2. Pregnancy
    If one has toxoplasma and then becomes pregnant it has no effect but the other way around can cause a serious disease for the foetus - in second and third trimester it can cause mental impairment and blindness in particular
  3. If infected with HIV
    Can have cysts lodging in the brain and encephalitis
112
Q

Toxoplasmosis

  1. Distribution
  2. Symptoms
  3. Diagnosis
  4. Treatment
  5. Disease control
  6. Immunity
A
  1. Worldwide
  2. Asymptomatic; CNS lesions, ocular disease in HIV
  3. Serology
  4. Often nil; antibiotics (eg bactrim)
  5. Well cooked food, avoid cats
  6. Lifelong infection
113
Q

What are 3 major types of Helminths?

A

Roundworm
Tapeworms
Flukes

114
Q

Name 3 common roundworms?

A

Pinworms Ascaris Strongyloides

115
Q

Name a common fluke

A

Schistosoma

116
Q

Name 2 common tapeworms

A

Echinococcus Taenia

117
Q

What species do roundworms (nematodes) infect?

What kind of animal are they are where are most foudn?

A

Major pathogens of humans and livestock
Tube-like animal, covered with cuticle
Most are free-living

118
Q

Who is primarily affected by Enterobius vermicularis (pinworm)

A

Most children infected at some time; highly contagious

119
Q

What is the life cycle of the Enterobius vermicularis (pinworm)

A

1cm long female crawls out of anus at night to release eggs
Fingers, sheets contaminated
Embryonated eggs are then ingested by human
Larvae hatch in the small intestine
Adults migrate to the lumen of the cecum
Female migrates to the perianal canal at night to lay eggs

120
Q

Enterobius vermicularis (pinworm)

  1. Distribution
  2. Symptoms
  3. Diagnosis
  4. Treatment
  5. Immunity
A
  1. Worldwide
  2. Many asymptomatic. Perianal/vaginal itch
  3. Detection of eggs (sticky tape)
  4. Antihelminthic (infection will go away in 4-6 weeks with good hygiene)
  5. Repeated and chronic infections occur
121
Q

Who is primarily affected by Ascaris lumbricoides (large intestinal roundworm)?

A

25% of the world’s population are affected

122
Q

What is the lifecycle of the Ascaris lumbricoides?

A

Unfertilized eggs are excreted in the feceas
The eggs are fertilized and mature in damp soil for a period of 4-5 weeks
The Eggs are then swallowed and develop in the gut
Once they have reached maturation they migrate through the hepatic circulation and into the lung.
They climb up the lung and are swallowed again (this is required for sexual maturation
Females are able to lay 200,000 eggs per day

123
Q

What causes pathology in Ascaris lumbricoides?

A

Pathology associated with larval migration and worms in intestines

124
Q

Is lyme disease found in Austrlian ticks?

A

No - should only be a clinical consideration if someone has been overseas

125
Q

Ascaris lumbricoides

  1. Distribution
  2. Symptoms
  3. Diagnosis
  4. Treatment
  5. Disease control
  6. Immunity
A
  1. Worldwide - esp in the tropics
  2. Many asymptomatic. Pneumonitis (larval migration),intestinal obstruction (pancreatitis, cholangitis etc) may be a cause of asthma in areas where it is endemic
  3. Eggs in faeces, imaging of obstructions
  4. Antihelminthic (Paralyse the worms and are then passed with the faeces)
  5. Sanitary sewage disposal
  6. Repeated and chronic infection occur
126
Q

What is the lifecycle of strongyloides stercoralis?

A

Larvae are extreted in stool
Develop in free living adults
Fertilization of eggs which hatch outside the body
Infective filariform larvae penetrate the skin and initiate infection
Filariform larvae are carried via the lungs to the trachea and finally swallowed and mature in intestine
Eggs are deposited in the intestinal mucosa, they hatch and migrate to lum
Larvae in the intestine can then exit the body or undergo autoinfection

127
Q

When are Strongyloides stercoralis especially dangerous?

A

They can become coated in gram negative bacteria which may cause serious infection if the person is immunosuppressed (i.e. from steroids)

128
Q

What causes the a pathology in Strongyloides stercoralis?

A

Pathology associated with larval migration and secondary bacterial infection

129
Q

Strongyloides stercoralis

  1. Distribution
  2. Symptoms
  3. Diagnosis
  4. Treatment
  5. Disease control
  6. Immunity
A
  1. Worldwide esp in the tropics
  2. Many asymptomatic. Pneumonitis (larval migration), disseminated/hyperinfection (do not get obstruction)
  3. Eggs in faeces, serology (good serological test)
  4. Antihelminthic
  5. Sewage disposal, shoes
  6. Repeated and chronic infections occur
130
Q

What are some common features of flukes?

A

• All parasitic • No body segmentation • Surface tegument • Blind gut • Organs in parenchyma

131
Q

What is the lifecycle of Schistosoma mansonii (Bilharzia) ?

A

Excreted through the feces
Eggs hatch releasing miracidia
Miracidia penetrate snail tissue
Develops and then released by snail into water (it is free swimming) - called a cercariae
Penetrates human skin
Cercariae lose tails during penetration
Migrate to portal blood in liver and mature into adults
Paired adult worms migrate to mesenteric venules of rectum and lay eggs which exit in the feces

132
Q

Schistosoma mansoni

  1. Distribution
  2. Symptoms
  3. Diagnosis
  4. Treatment
  5. Disease control
  6. Immunity
A
  1. Africa, tropical South America, Caribbean
  2. Causes a non specific febrile ilness, eggs can travel through various tissues and lodge in organs. It can cause hepatitis (hepatomegaly). Can also cause portal hypertension and associated pathogenesis
  3. Characteristic eggs in faeces, serology
  4. Antihelminthic (effective - no resistance)
  5. Snail control (molluscacides), sanitary disposal of sewage, treatment of carriers
  6. Persistent infections and reinfections are common, concomitant immunity can be demonstrated in animal hosts, immune evasion by immunological masking
133
Q

What are some common characteristics of tapeworms?

A

• All parasitic. • Segmented body. • Surface tegument. • No gut. • Organs in parenchyma
They cause most of their disability as a result of metabolic consumption - they consume huge amounts of nutrients

134
Q

What is the life cycle of Echinococcus granulosus?

A 
Embyonated eggs are released in feaces
Oncosphee hatches and pentrates intestinal wall (ingestion of cysts occurs in dogs and other canidae, in other species it is ingested through eggs and cannot fully mature)
Hypatid cysts (larval cycsts) form in lungs, liver etc
Proliferation internally in cysts produces infected protoscoleces 
Scolex attaches to intestine 
Adult in intestine produces eggs
135
Q

Are humans definitive hosts of Echinococcus granulosus?

A

No, Humans are accidental intermediate hosts

136
Q

Epidemiology of Echinococcus granulosus

A

Endemic in: N.S.W., A.C.T., Queensland, Victoria, S.A. and W. A.
• Eradicated in Tasmania
• Notifications

137
Q

Echinococcus granulosus

  1. Distribution
  2. Symptoms
  3. Diagnosis
  4. Treatment
  5. Disease control
  6. Immunity
A
  1. Worldwide
  2. Hydatid cysts in tissues principally in liver and lungs but may occur in any body site, symptoms vary with number, size and location of cysts
  3. Imaging techniques (CT MRI), serology
  4. Surgery (for big worms), PAIR (fluid removed from cyst), antihelmintics (Cysts are very reactogenic - they can cause a severe hypersensitivity, thus surgery can be dangerous)
  5. prevention of infection in dogs, public education, personal hygiene, quarantine of infected livestock, vaccination in livestock
  6. concomitant immunity, vaccination induces protection against egg infection*
138
Q

What is Taeniasis?

A
  • Zoonotic infection
  • Humans can be both definitive and intermediate hosts
  • Tapeworm up to 10m long
  • Eat undercooked meat from animal infected with tapeworm
  • Major cause of neurological disease in endemic countries (acquired epilepsy)
139
Q

Life-cycle of taeniasis

A

Eggs are passed into the environment via the feces
Cattle (T. saginata) and pigs (T.solium) becoem infected by ingesting the eggs
Eggs hatch and Oncospheres circulate in the musculature
Develop cysticeri in muscle
Huamns eat infected and undercooked meat
Attachemen to intestine
Adults develop in small intestine and produce eggs or gravid proglottids

140
Q

Taenia solium

  1. Distribution
  2. Symptoms
  3. Diagnosis
  4. Treatment
  5. Disease control
  6. Immunity
A
  1. Africa, Latin America, Asia
  2. Cysts (cysticerci) in subcutaneous and neural tissues
  3. Serology, imaging techniques
  4. Anthelmintics (caution)
  5. Treatment of carriers, avoidance of eating raw pork, sanitary disposal of sewage, personal hygiene, vaccination in pigs
  6. Concomitant immunity, vaccination induces protection against egg infection

GIT (15 decks)

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